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Related Concept Videos

Aging01:26

Aging

Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
The Effect of Aging on Tissues01:19

The Effect of Aging on Tissues

Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...
Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...

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Related Experiment Video

Updated: May 10, 2026

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression
07:30

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression

Published on: June 15, 2019

A Sepsis-Informed Model of Accelerated Aging.

Michelle Kabakibi1, Julie-Kathryn Graham1

  • 1San Diego State University School of Nursing, 5500 Campanile Drive, San Diego, CA 92182, USA.

Critical Care Nursing Clinics of North America
|May 8, 2026
PubMed
Summary
This summary is machine-generated.

Aging and sepsis share cellular impacts, particularly involving toll-like receptor 4 (TLR4) immune dysregulation. A new model of aging is proposed, inspired by the 2024 OO(H)NO! sepsis model, to explain these shared TLR4 dysregulation mechanisms.

Keywords:
Immunologic dysregulationMetabolic dysregulationSepsis and agingTLR4 dysregulation

More Related Videos

Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

Related Experiment Videos

Last Updated: May 10, 2026

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression
07:30

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression

Published on: June 15, 2019

Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

Area of Science:

  • Immunology
  • Gerontology
  • Cellular Biology

Background:

  • Sepsis and aging exhibit overlapping immunological dysregulation.
  • Toll-like receptor 4 (TLR4) pathway activity is implicated in both conditions.

Purpose of the Study:

  • To review the literature for shared cellular impacts between sepsis and aging.
  • To propose a novel model of aging based on sepsis pathophysiology.

Main Methods:

  • Literature review and synthesis.
  • Conceptual modeling based on existing data.

Main Results:

  • Evidence supports shared immunologic dysregulation in sepsis and aging, particularly concerning TLR4.
  • A new conceptual model for aging is proposed, mirroring the OO(H)NO! model of sepsis.

Conclusions:

  • TLR4 dysregulation is a key shared mechanism between sepsis and aging.
  • The proposed aging model offers a framework for understanding age-related immune dysfunction and its parallels with sepsis.